Chemoreceptor nerve activity may not be proportional to catecholamine secretion in rat carotid body. Donnelly, David F. Department of Pediatrics, Section of Respiratory Medicine, Yale University School of Medicine, New Haven, CT 06510
APStracts 3:0131A, 1996.
Enhanced catecholamine secretion from the carotid body glomus cells is hypothesized to play an essential role in mediating the peripheral chemoreceptor response to hypoxia. To tests aspects of this hypothesis, the relationship between catecholamine secretion and nerve activity was examined during repetitive hypoxia stimuli and following catecholamine depletion with reserpine. Single-fiber afferent nerve activity was measured along with an estimate of free -tissue catecholamine using Nafion-coated carbon-fiber microelectrodes placed in rat carotid bodies, in vitro. Baseline and stimulated nerve and catecholamine levels were quantified during repetitive stimulation (anoxia of 1min duration; PO2=0 Torr, at nadir, repeated each 200 sec). Peak stimulated catecholamine progressively decreased from 26.4+/-2.6 [mu]M for the first stimuli to 7.5+/-0.9 [mu]M for the 5th stimuli (N=15), but peak nerve activity was much less affected (23.0+/-1.9 Hz, 1st trial; 19.9+/-1.4 Hz, 5th trial). An exposure to moderate hypoxia (about 80 Torr), prior to the repetitive anoxia stimuli, produced catecholamine levels comparable to that obtained during anoxia, but peak nerve activity was significantly less (22.5+/-3.4 Hz vs 12.7+/-2.1 Hz). Pretreatment with reserpine (1mg/100g) resulted in a large reduction in the average catecholamine response (1.4+/-0.3 [mu]M, N=9), but peak nerve activity was not different than non-treated controls. These results demonstrate an independence between carotid body catecholamine secretion and nerve activity, suggesting that hypoxia transduction is, at least, partially mediated through pathways independent of granule secretion. 

Received 22 May 1995; accepted in final form 20 February 1996.
APS Manuscript Number A528-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 13 March 96